A gene that is known to play a key role in suppressing cancer also seems to protect against sun damage while promoting a golden tan.

The revelation could one day lead to better ways to prevent skin cancer, which roughly 1 million Americans develop each year.

"This finding provides us an opportunity to look at human populations with a varied risk of developing skin cancer and start to identify precisely what is regulating the risk of developing skin cancer rather than estimating," said senior study author Dr. David Fisher, director of the melanoma program at the Dana-Farber Cancer Institute at Harvard Medical School. "Right now, we're incredibly inaccurate in identifying risk and, therefore, in ameliorating risk."

The findings are published in the March 9 issue of Cell.

People who tan easily or have darker skin are much less likely to develop melanoma, the deadliest form of skin cancer.

"The tanning response is a protective response to injury, which can prevent further injury," explained Dr. Robin Ashinoff, medical director of Dermatologic, Mohs and Laser Surgery at Hackensack University Medical Center, in New Jersey. "On the one hand, the skin is the most common organ to be affected by cancer and, in principle, it ought to be preventable because we know the carcinogen which causes it, the sun."

Still, rates of skin cancer remain high.

"That's a terrible state of affairs in 2007," Fisher said. "We really want to understand the impact of ultraviolet radiation on the skin and what is the molecular cascade that is occurring downstream."

Six months ago, Fisher and his team published a paper documenting the fact that keratinocytes -- cells closer to the surface of the skin -- react to sun exposure. Previously, it had been thought that pigment-producing melanocytes played this role.

Once keratinocytes are exposed to rays from the sun, they produce melanocyte-stimulating hormone (MSH), a growth factor which binds to the pigment cells (melanocytes) and stimulates them to produce pigment.

Differences in the MSH receptor explain differences in ability to tan. Redheads, for example, have a variant which doesn't respond at all to MSH, explaining why the Nicole Kidmans of this world don't turn a tawny bronze.

Fisher and his colleagues still didn't know, however, what happened within keratinocytes to stimulate MSH production.

"We knew that ultraviolet radiation causes MSH to be induced," Fisher said. "How is the ultraviolet radiation doing that? What is perceiving the radiation and translating that signaling into making more MSH?"

The key happens to be the tumor-suppressor gene known as p53, which is induced in almost every keratinocyte of human skin samples within an hour of being exposed to the sun's ultraviolet rays. "That activity is completely regulated by this protein," Fisher said.

The finding is biologically plausible, experts said.

"It makes sense that most skin cancers and cancers, for that matter, have mutations in the p53 because it functions to protect us. It basically causes abnormal cells to be killed or die, and regulates all sorts of pathways that protect us," Ashinoff said. "It's not surprising that something that would protect us would also stimulate mechanisms in the skin known for protecting us."

"Knowing this, we can now identify exactly where we would like to interfere with the risk," Fisher added. "Knowing that p53 is part of this process allows us to potentially identify drugs that might be able to restore this response at different steps, depending on where the person might need it, where their block is."